[The use of tissue expanders in mandibular reconstruction].
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Equipment Design↗
Biomedical subjects
M Giordano
Publications and source records attributed to M Giordano.
Bistability phenomena in electron paramagnetic resonance.
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Journal Article↗
Expression of genes of ferritin subunits in human hepatoma cell lines.
The expression of ferritin genes has been studied in two well differentiated hepatoma cell lines, HepG2 and Hep3B, and in an undifferentiated cell line, HepPLC/PRF/5. The steady-state level of the H and L ferritin subunit mRNAs is different in the three cell lines, being most abundant in the HepG2 and Hep3B cells. The efficiency of promotion of transcription of the H and L gene promoters is not correlated with the levels of the two transcripts; moreover the half-life of the H and L mRNAs varies among the hepatoma cells. The different level of ferritin mRNAs in differentiated and undifferentiated cells appears to be mainly due to a different stability of the transcripts.
Blotting, Northern↗
Neuroleptic-induced emotional defecation: effects of scopolamine and haloperidol.
Most investigators have found a decrease in emotional defecation in rats given neuroleptics in novel environments, supporting their action as a major tranquilizer. We have found, however, that in rats a profound increase in emotional defecation can result from neuroleptic administration in well habituated environments, such as the homecage. Anticholinergics are known to be effective in treating the side effects associated with neuroleptic administration in humans. Therefore the present study determined the effects of anticholinergic treatment in this animal model. In male rats, defecation was measured for a 1-h test period in their homecage following various doses of the central and peripheral anticholinergics, scopolamine, and n-methylscopolamine, respectively. A decrease in fecal excretions and an attenuation of haloperidol-induced defecation was found following administration of scopolamine. n-Methylscopolamine reduced defecation at all doses. When n-methylscopolamine was combined with haloperidol, both fecal mass and number decreased significantly. Since both anticholinergic agents reduced haloperidol-induced defecation it is suggested that their effectiveness is mediated through peripheral mechanisms.
Animals↗
The quinolinic acid model of Huntington's disease: locomotor abnormalities.
In contrast to other excitotoxins, such as kainic acid, quinolinic acid (QA) may spare a specific population of striatal neurons that is also spared in Huntington's disease (HD). Although several histological and biochemical experiments support the use of QA as a model for HD, to date no behavioral experiments have been performed to examine the suitability of this model. The present study explored the behavioral effects of bilateral intrastriatal microinjections of four doses (75, 150, 225, 300 nmol) of QA in the male rat. Using a multidimensional analysis of spontaneous locomotion (Digiscan activity) and a record of metabolic indicators, such as weight loss, a dose-dependent effect was found. The 75-nmol dose had no significant effect on locomotion or feeding behavior. In contrast, the 150- and 225-nmol doses induced hyperactivity and weight loss, whereas the 300-nmol dose was lethal. The results obtained suggest that striatal injections of 150-225 nmol of QA induce behavioral deficits qualitatively similar though quantitatively less than those which are seen after similar injection of 3 nmol of kainic acid and which have been reported to be comparable to the symptomatology of HD. Together with QA's possible greater histological selectivity, the present results support the use of QA-induced striatal lesions as a behavioral model of Huntington's disease.
Animals↗
Fetal striatal tissue grafts into excitotoxin-lesioned striatum: pharmacological and behavioral aspects.
In an excitotoxin animal model of Huntington's disease (HD), fetal striatal tissue transplants survive and grow in the host brain and reverse the behavioral, and, hence, functional deficits produced by the lesion. In the present study we found recovery of apomorphine-induced rotation behavior in unilateral excitotoxin-lesioned rats indicating that the transplant reverses this functional pharmacologic deficit induced by the lesion. It might, therefore, by expected that the transplanted fetal striatal tissue would possess similar pharmacological characteristics as the host striatum. However, autoradiographic localization of D1 and D2 dopamine receptors demonstrated that the transplanted tissue expressed relatively small numbers of these receptor subtypes. Furthermore, there was a relative deficit of [3H]forskolin binding to the stimulatory guanine nucleotide regulatory subunit/adenylate cyclase complex in the fetal striatal tissue transplants. Therefore, transplanted tissue which is neurochemically dissimilar to the host striatum is capable of reversing deficits in both drug-induced and spontaneous locomotor activity.
Adenylyl Cyclases↗
Lymphocyte proliferative response to mitogenic monoclonal antibodies in systemic sclerosis. Evidence for unresponsiveness to murine monoclonal antibodies of IgG1 isotype.
Proliferative response of peripheral blood mononuclear cells to phitohemoagglutinin and anti-CD3 mitogenic monoclonal antibodies (MoAbs) of the IgG2a (OKT3) and IgG1 (PanT2, CLB T3/4.1) isotypes was studied in 39 patients with systemic sclerosis (SSc) and in 82 control subjects. The effect of IL-2 on this response was also investigated. No difference in the response to PHA and to IgG2a anti-CD3 MoAb OKT3 was seen between scleroderma patients and controls. Both the patient and control groups contained responders and non-responders to IgG1 anti-CD3 MoAbs. The percentage of non-responders was significantly higher in scleroderma patients than in controls. When purified lymphocytes from non-responder scleroderma patients were cultured with monocytes from control responders, proliferative response to IgG1 MoAbs was restored. Our results show that monocytes from patients with systemic sclerosis bear a defect leading to IgG1 unresponsiveness by T lymphocytes.
Adolescent↗
[Holiday heart syndrome: spontaneous reversibility of the electrocardiographic and echocardiographic alterations].
The holiday heart syndrome is characterized by symptomatic arrhythmias more often supraventricular, elicited by alcohol ingestion, typically during the week-end period. After admission, electrocardiographic changes, which disappear in few days, are often reported. A case of an alcoholic with syncopal episodes related to alcohol ingestion is described. In this patient, remarkable changes of ventricular repolarization on the electrocardiogram associated with impairment of ventricular diastolic function on the Doppler echocardiographic study are showed. ECG and echo-Doppler data reversed to normality after few days of alcohol withdrawal.
Alcoholism↗
[Interaction of immune complexes and their leukocyte receptors: regulation by the complement system and by cyclophosphamide].
During the course of this investigation we have studied different aspects related to the interaction between immune complexes (CI) and their cellular receptors for the Fc-fragment of IgG (RFc gamma). Our first approach was to demonstrate that the alternative pathway of complement is the main one responsible for the CI-dissociation from their receptors of human peripheral mononuclear cells. This modulatory effect was studied throughout the functional restoration of antibody dependent cellular cytotoxicity (CCCDA), which is a mechanism susceptible to Cl-inhibition. The results suggest that the levels of circulating Cl do not necessarily correlate with the tissue damage they produce. Secondly, we have demonstrated that cyclophosphamide (Cy), which is a potent immunomodulating drug which has been used for the treatment of diseases characterized by high levels of Cl, enhances the capacity of the mononuclear phagocytic system to remove IgG-particulate complexes in mice. Finally, we have described a nonspecific cytotoxic system triggered by Cl against different target cells, through a mechanism that involves the reactive metabolites of O2.
Animals↗
[Traumatic laceration of facial nerve and Stenone duct. A clinical case].
After a brief review of the main operating techniques employed in the reconstruction of the facial nerve and Stenone's duct lacerated by trauma, a clinical case in which the two lesions are associated is reported. Suture of the lacerated nervous branches and attachment of the salivary fistula to the oral mucosa using a silicon drainage applied for a few days permitted functional recovery of neuronal activity and salivation.
Adolescent↗
Proliferative pathways in CD1- CD3+ CD4+ CD8+ T-prolymphocytic leukemic cells: analysis with monoclonal antibodies and cytokines.
The antigenic profile and the proliferative pathways in leukemic cells from the patient TRT with T-prolymphocytic leukemia (T-PLL) were analyzed using monoclonal antibodies (MoAbs) and cytokines. T-PLL cells expressed the phenotype CD1- CD3+ CD4+ CD8+. Incubation with the differentiating agent phorbol-12-myristate-13-acetate markedly increased the percentage of cells with the CD4- CD8+ phenotype, suggesting that leukemic cells were already committed towards a differentiated element with the CD4- CD8+ phenotype. T-PLL cells were induced to proliferate by anti-CD2 MoAb 9-1 + 9.6 and by anti-CD3 MoAb OKT3. The two pathways exhibited normal functional interactions and were susceptible to modulation by anti-HLA class I MoAbs. These results indicate that regulation of cell proliferation was preserved to a significant extent in the T-PLL cells analyzed. At variance with normal resting T cells that require previous activation to proliferate when incubated with interleukin-1 (IL-1) or interleukin-2 (IL-2), T-PLL cells proliferated vigorously when incubated with either interleukin. Furthermore, T-PLL cells proliferated when incubated with immune interferon (IFN-gamma). The latter finding parallels the enhancement by IFN-gamma of the proliferative response of lectin-activated murine T lymphocytes. These results suggest that T-PLL cells, which express a high constitutive level of c-myc mRNA, may be in an activated state. The antigenic phenotype and the characteristics of the proliferative pathways of T-PLL cells from the patient TRT are compatible with the possibility that they may be derived from an intermediate thymocyte.
Antibodies, Monoclonal↗
Double-modulation electron-spin-resonance spectroscopy: Experimental observations and theoretical comprehensive interpretation.
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Journal Article↗
Intraparenchymal fetal striatal transplants and recovery in kainic acid lesioned rats.
Striatal kainic acid (KA) lesions induce behavioral and biochemical deficits which resemble symptoms encountered in patients suffering from Huntington's disease. In rats with KA lesions, fetal striatal transplants have shown to reverse the pervasive nocturnal hyperactivity induced by the lesion. In the present study 4.6 mm3 of fetal striatal tissue were delivered bilaterally into the anterodorsal portion of the lesioned caudate nucleus. Care was taken to deliver the transplant within the host parenchyma and away from the lateral ventricles. Locomotor behavior analyzed using the Digiscan animal activity monitors before and after the transplants demonstrated a reversal of the hyperactivity following transplants in 70% of lesioned animals. Microinjections of horseradish peroxidase delivered into the globus pallidus and substantia nigra of a small group of functionally recovered transplanted animals, did not reveal evidence for reinnervation between host nigra or pallidum and the transplant at 10 weeks post-transplantation. Other laboratories have reported anatomical connections by 6 months post-transplantation. Ventricular/brain ratios demonstrated that intraparenchymal transplants significantly reduced the ventricular dilation following KA lesion. These results suggest that functional recovery can be obtained when the transplant is immersed into the host's striatal parenchyma regardless of the existence of long-range anatomical connections.
Animals↗
[Clinical and microscopic study of a photopolymerizing composite].
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Composite Resins↗
In vivo bromodeoxyuridine incorporation in human gastric cancer: a study on formalin-fixed and paraffin-embedded sections.
Bromodeoxyuridine (BUDR) is a non-radioactive thymidine analogue which is incorporated into the DNA of proliferating cells. This allows evaluation of the size of the S-phase as the BUDR labelling index (BUDR-LI) not only in vitro but also in vivo, since BUDR is not toxic at the doses needed to label cells. To ascertain whether in vivo BUDR incorporation can be detected on routine histological material we tested several different procedures prior to immunoperoxidase staining, on formalin-fixed, paraffin-embedded sections from five patients with gastric cancer, who received BUDR (250 mg m-2, intravenous) 4 h before surgery. To determine the optimal conditions for detecting BUDR in formalin-fixed tissues, immunohistochemical testing for BUDR was performed simultaneously on duplicate sections fixed with 70% ethanol. It was found that hydrolysis with 3N HCl at 37 degrees C for 30 min and digestion with 0.5% in at 37 degrees C for 30 min were sufficient to detect BUDR immunoreactivity in formalin-fixed sections. The method presented extends the range of applications of the in vivo BUDR technique for cell kinetics studies in human neoplasms because it can be used on routinely fixed archival material, with the advantage of correlating the kinetic data with histopathological characters.
Adenocarcinoma↗
Neural transplants disrupt the blood-brain barrier and allow peripherally acting drugs to exert a centrally mediated behavioral effect.
The disruption of the blood-brain barrier (BBB) following neural transplantation has been demonstrated with horseradish peroxidase histochemistry. It appears that the BBB becomes at least temporarily permeable to large macromolecules. In this study, two drugs (N-methylscopolamine and domperidone) that do not normally cross the BBB were shown to exert a centrally mediated behavioral effect when systematically administered in transplanted rats. This demonstrates that N-methylscopolamine, domperidone, and perhaps other peripherally acting drugs can enter the brain via transplants and directly modify CNS function.
Animals↗
Striatal tissue transplants attenuate apomorphine-induced rotational behavior in rats with unilateral kainic acid lesions.
Four to six weeks following unilateral striatal kainic acid (KA) lesions, challenge with apomorphine (0.5-0.75 mg/kg s.c.) elicited rotational behavior. Gestational day 17-19 rat fetal striatal tissue was implanted into the lesioned striatum, and rats were rechallenged with apomorphine 10 weeks post-transplant. There was a significant reduction in the maximal rate of rotations and an alteration in the topography of locomotor activity in response to apomorphine. These data indicate that the transplanted material may possess similar pharmacological properties as the original host tissue and is capable of functionally repairing damage to a complex neurochemical system.
Animals↗
Different requirements for the induction of antibody-dependent and immune complexes triggered cytotoxicity mediated by monocytes.
We have previously shown that immune complexes triggered nonspecific cytotoxicity (NSC) towards nonsensitized target cells and antibody-dependent cellular cytotoxicity (ADCC), two functions mediated through monocyte Fc gamma receptors, employing different lytic mechanisms [Geffner, J. R., et al. (1986) Clin. Exp. Immunol. 67, 646]. In this report, we analyze some of the metabolic requirements involved in the induction of monocyte NSC and ADCC. The results showed NSC to be dependent on: (1) metabolic energy derived from glycolysis, (2) availability of external Ca2+, (3) calmodulin activity, (4) integrity of microtubules, but not the microfilament system, and (5) activation of phospholipase(s) and lipoxygenase. On the other hand, ADCC was not impaired by: (1) inhibition of glycolysis, (2) Ca2+ chelation, (3) disruption of microtubules, or (4) inhibition of calmodulin or lipoxygenase. It is concluded that monocyte NSC and ADCC are regulated by different endogenous signals.
Antibody-Dependent Cell Cytotoxicity↗